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Pancreatic cancer is one of the major human malignant tumors severely endangering human health and life with high mortality due to the concealment of early symptoms and lack of effective therapies during advanced stages. The identification of pancreatic cancer stem cell functions has been as important strategy for understanding of pancreatic cancer biology and novel drug and therapy development. In the present study, we successfully isolated the pancreatic sphere-forming cells from pancreatic cancer cell line PANC-1 by sphere-forming method and we found that the sphere-forming ability and the cell migration rate of pancreatic sphere-forming cells were significantly inhibited by 5,7-DMF treatment, which was supported by the corresponding changes of several EMT biomarkers after being treated with 5,7-DMF. Moreover, we revealed here that the inhibition of pancreatic sphere-forming cells was mediated by the expression of FoxM1 gene, and also the expression of SOX2 gene was regulated by FoxM1 in pancreatic sphere-forming cells and involved in the inhibitory role of 5,7-DMF. These results provided important basis for the application of 5,7-DMF as a novel drug candidate for the pancreatic cancer treatment.
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http://dx.doi.org/10.1002/jcb.26346 | DOI Listing |
Cell Commun Signal
June 2025
Children's Cancer Institute, Lowy Cancer Research Centre, UNSW Sydney, Sydney, NSW, Australia.
Background: Extracellular vesicles (EVs) play a crucial role in intercellular communication. While the effects of EVs released from living or non-dying cancer cells are well characterized, the impact of EVs released from chemotherapy-treated or apoptotic cancer cells is less understood. This study investigated the effects of the chemotherapy agent cisplatin on EV release and miRNA content in apoptotic medulloblastoma cells, as well as their influence on the growth of drug-naïve recipient cancer cells.
View Article and Find Full Text PDFBiochem Pharmacol
September 2025
Guangzhou Key Laboratory of Formula-Pattern Research Center, School of Traditional Chinese Medicine, Jinan University, Guangzhou 510632, PR China. Electronic address:
Pancreatic cancer is a highly aggressive malignancy with poor prognosis and high mortality rates. KRAS mutations are ubiquitous in pancreatic cancer, driving tumorigenesis by promoting uncontrolled cell proliferation, survival, and metastasis. Therefore, identifying therapeutic agents effective against KRAS-mutant pancreatic cancer is urgently needed.
View Article and Find Full Text PDFFront Cell Dev Biol
February 2025
Donnelly Centre for Cellular & Biomolecular Research, University of Toronto, Toronto, ON, Canada.
Previously isolated adult pancreatic precursors called pancreatic multipotent progenitors (which make both pancreatic endocrine and exocrine cell types) originate from the Pancreatic Duodenal Homeobox 1 (PDX1) pancreatic developmental lineage. The embryonic time point at which adult pancreatic multipotent progenitor cells emerge has not been established. We have employed the use of two models: a human embryonic stem cell (hESC) to beta-cell cytokine-induced differentiation protocol and a mouse lineage tracing model during early development to isolate clonal pancreatic spheres.
View Article and Find Full Text PDFDiscov Med
February 2025
Department of Oncology, Hunan Provincial People's Hospital, 410002 Changsha, Hunan, China.
Background: Exploring the pathological mechanism of colorectal cancer (CRC) onset and advancement is critical to clinical diagnosis and treatment. In this context, our study brings a novel perspective by investigating the role and regulatory mechanism of E74 Like ETS Transcription Factor 1 () in CRC, a topic that has not been extensively explored.
Methods: Quantitative reverse transcription polymerase chain reaction (RT-qPCR) and western blotting (WB) assays were used to detect the expression of ELF1 in CRC cells.
PLoS One
December 2024
Department of Biliary-Pancreatic Surgery, Affiliated Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
B3GNT5, a critical member of the β-1,3-N-acetylglucosaminyl transferase gene family involved in lactose and glycosphingolipids biosynthesis, has been documented to promote tumor-infiltrating T-cell responses. Our research utilized the Pan-Cancer dataset from The Cancer Genome Atlas (TCGA) to explore the functional role of B3GNT5. Our study demonstrated that the antibody-driven inhibition of B3GNT5 diminished T cell-mediated anti-tumor responses in both in vitro and in vivo settings.
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